Rac1-Mediated DNA Damage and Inflammation Promote Nf2 Tumorigenesis but Also Limit Cell-Cycle Progression
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- 作者：Yuhao Shi1 ; 3 ; Saumya R. Bollam1 ; 3 ; Shannon M. White1 ; Sean Z. Laughlin1 ; Garrett T. Graham1 ; Mandheer Wadhwa1 ; Hengye Chen1 ; Chan Nguyen1 ; Jeremie Vitte2 ; Marco Giovannini2 ; Jeffery Toretsky1 ; Chunling Yi1 ; 4 ; cy232@georgetown.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：NF2 ; Rac1 ; Yap ; senescence ; ROS ; inflammation ; DNA damage response
- 刊名：Developmental Cell
- 出版年：2016
- 出版时间：21 November 2016
- 年：2016
- 卷：39
- 期：4
- 页码：452-465
- 全文大小：7844 K
文摘
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Rac1 is required for tumorigenesis but limits hepatomegaly induced by Nf2 loss
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Rac1 induces inflammation and senescence in response to Nf2 deletion in the liver
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Benign human NF2 tumors express senescence-associated genes
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Yap is the ultimate driver of cell cycle and proliferation in Nf2-deficient livers